Hirudin protects against kidney damage in streptozotocin-induced diabetic nephropathy rats by inhibiting inflammation via P38 MAPK/NF-κB pathway
Mechanism study published in Drug Design, Development and Therapy (2020)
Abstract
BACKGROUND: Inflammation-induced podocyte apoptosis plays an important role in kidney injury during diabetic nephropathy (DN). Hirudin (HIR), a natural compound extracted from leeches, can inhibit inflammation. However, whether HIR can protect the kidneys against inflammation during DN is unknown. In the present study, we aimed to study the effects of HIR on kidney damage in a DN rat model and explore its anti-inflammatory properties. METHODS: A streptozotocin-induced DN rat model was generated, and HIR was administered subcutaneously. Immortal podocytes and primary peritoneal macrophages were used for vitro studies. Hematoxylin and eosin staining was used to evaluate renal pathological changes; quantitative polymerase chain reaction and immunoblotting were used to detect gene expression; and TUNEL staining was used to detect apoptotic cells. RESULTS: Our results showed that HIR protected against renal injury, as indicated by kidney weight/body weight, serum creatinine, renal pathological changes, blood urea nitrogen, and detection of urine proteins. Notably, HIR treatment reduced macrophage infiltration, pro-inflammatory cytokine expression, and podocyte apoptosis in the kidney tissues of DN rats. In vitro, high glucose (HG) induced the activation of M1 macrophages, which was accompanied by increased podocyte apoptosis. HIR could decrease HG-induced podocyte apoptosis and suppress pro-inflammatory cytokine expression in podocytes in vitro. This was achieved via inhibition of p38 MAPK/NF-κB activation in renal tissues and podocytes. CONCLUSION: HIR could inhibit inflammation via the p38 MAPK/NF-κB pathway, prevent podocyte apoptosis, and protect against kidney damage in a DN rat model.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
Hirudin protects against renal damage in STZ-diabetic rats by inhibiting inflammation via P38 MAPK/NF-κB pathway — mechanistic basis for leech-hirudin anti-inflammatory action.
Por qué esto importa para la hirudoterapia
Este estudio examinó si la hirudina (HIR), un compuesto extraído de sanguijuelas, podría proteger contra el daño renal en un modelo de rata con nefropatía diabética (ND) inducida por estreptozotocina, mediante la inhibición de la inflamación a través de la vía p38 MAPK/NF-κB. La hirudina redujo la infiltración de macrófagos, la expresión de citocinas proinflamatorias y la apoptosis de podocitos en riñones de ratas con ND; in vitro, disminuyó la apoptosis de podocitos inducida por alta glucosa y suprimió la expresión de citocinas proinflamatorias en podocitos, logrado mediante la inhibición de la activación de p38 MAPK/NF-κB en tejidos renales y podocitos. Esto es relevante para el ámbito de ASH, ya que investiga las propiedades antiinflamatorias y renoprotectoras de un compuesto extraído de sanguijuelas en un modelo de enfermedad. Sin embargo, todos los hallazgos derivan de un modelo de ND en rata y de estudios celulares in vitro; no se presentan datos de dosificación, seguridad ni eficacia en humanos.
Citación
Hirudin protects against kidney damage in streptozotocin-induced diabetic nephropathy rats by inhibiting inflammation via P38 MAPK/NF-κB pathway.
Han J et al. · Drug design, development and therapy, 2020
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026